1. Increases in plasma erythropoietin and erythropoietin receptor activation are mechanisms implicated in the increase of plasma FGF23 in acute kidney injury. PMID: 29395333
2. In chronic kidney disease (CKD) rat models, FGF23 mRNA is expressed in the kidney, and the FGF23 protein is expressed at high levels in osteopontin-positive renal tubule epithelium cells likely via TGFbeta1 stimulation. FGF23 produced in the kidney might contribute to P metabolism in subjects with CKD. PMID: 29518087
3. High FGF23 expression is associated with cardiac hypertrophy. PMID: 28339837
4. The only direct contribution of the injured kidney to circulating FGF23 levels in uremia appears to be reduced renal extraction of bone-derived FGF23. PMID: 28341272
5. Osteoblast Fgf23 transcription is upregulated by increase in the cytosolic Ca(2+) activity. Fgf23 transcription is decreased by Orai inhibitors and Orai1 silencing. Fgf23 transcription is lowered by NFkappaB inhibitors. PMID: 26631141
6. EPO dependent regulation pathway of FGF23 gene expression PMID: 29073196
7. can directly stimulate hepatic secretion of inflammatory cytokines PMID: 27457912
8. dietary Mg deficiency causes a rapid increase in circulating levels of FGF23 and renal 24(OH)ase mRNA levels PMID: 27624533
9. phosphate directly enhances Fgf23 transcription without affecting the stability of Fgf23 messenger RNA. PMID: 25792238
10. Fgf23 gene transcription was abolished by the actin microfilament-disrupting agent cytochalasin B, as well as by the inhibition of actin-regulating Rac1/PAK1 signaling. PMID: 26878191
11. Although the molecular link between the cardiac lesion and circulating Fgf23 concentrations remains to be identified, our study has uncovered a novel heart-bone-kidney axis PMID: 25858796
12. In conclusion, PRL was responsible for the lactation-induced mucosal adaptations, which were associated with compensatory increase in FGF-23 expression probably to prevent calcium hyperabsorption. PMID: 26657069
13. Data indicate that serum fibroblast growth factor 23 (FGF-23) levels independently correlated with bone volume parameters in rats with experimentally induced chronic kidney disease (CKD). PMID: 26186634
14. fibroblast growth factor 23 is increased by intravenous phosphate loading in uremic rats PMID: 24625659
15. The polycystic kidney produces FGF23 but is resistant to its action. PMID: 24402093
16. FGF23 enhances phosphate-induced vascular calcification by promoting osteoblastic differentiation involving the ERK1/2 pathway in the absence of Klotho deficiency. PMID: 24088960
17. Ca is not a regulator of acute changes in FGF23 secretion. PMID: 24801007
18. data suggest that inhibition of FGFR signaling following administration of either pan-FGFR inhibitor or MEK inhibitor interferes with the FGF23 pathway, predisposing animals to hyperphosphatemia PMID: 23872713
19. In non-iron depleted normal and uremic rats a single high dose of either of two intravenous iron preparations, iron isomaltoside 1000, and ferric carboxymaltose, had no effect on plasma levels of iFGF23 and phosphate for up to seven days. PMID: 24373521
20. Mg deficiency increases serum FGF-23 levels. PMID: 23608165
21. a direct and an indirect effect of parathyroid hormone on FGF23 secretion, the latter through changes in calcitriol concentrations PMID: 21525854
22. late-onset ADHR is the product of gene-environment interactions whereby the combined presence of an Fgf23-stabilizing mutation and iron deficiency can lead to ADHR PMID: 22006328
23. FGF23 normalizes serum phosphate and decreases 1,25-dihydroxyvitamin D levels in early-stage chronic kidney disease. PMID: 20844473
24. Serum FGF23 increased in uremic rats treated with paricalcitol but not those treated with cinacalcet. PMID: 20200094
25. because of a downregulation of the Klotho-FGFR1c receptor complex, an increase of circulating FGF23 does not decrease parathyroid hormone levels in established chronic kidney disease. PMID: 20016468
26. Data indicate that cleavage at the RXXR motif abrogates FGF23 activity by removing the binding site for the binary FGFR-Klotho complex in the C-terminal region of FGF23, and by generating an endogenous inhibitor of FGF23. PMID: 19966287
27. a feedback loop exists among serum phosphorus, 1alpha,25(OH)(2)D(3), and FGF-23, in which the novel phosphate-regulating bone-kidney axis integrated with the parathyroid hormone-vitamin D(3) axis in regulating phosphate homeostasis PMID: 15531762
28. rat UMR-106 osteoblast-like cells were treated with 1,25(OH)(2)D(3) resulted in a dose- and time-dependent stimulation of FGF23 mRNA concentrations. PMID: 16020653
29. Mineralized tissue cells are a principal source of Fgf23. PMID: 17350357
30. FGF23 suppressed both parathyroid hormone (PTH) secretion and PTH gene expression PMID: 17992255
31. These results suggest that the N- and C-terminal domains of FGF23 are responsible for association with cognate FGF receptors and Klotho, respectively, and that these interactions are indispensable for FGF23 activity. PMID: 18442315
32. Results show that the elevated plasma FGF23 levels in uremic rats reflect the increased expression of FGF23 in bone. PMID: 19339809
33. estrogens regulate PTH indirectly, possibly through FGF23 PMID: 19628670

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KEGG: rno:170583

STRING: 10116.ENSRNOP00000026888

UniGene: Rn.154421